Differential Diagnosis of Metabolic Acidosis
Section snippets
Elevated anion gap acidoses
The elevation of the anion gap is created by inorganic (eg, phosphate, or sulfate), organic (eg, ketoacids or lactate), or exogenous (eg, salicylates) acids incompletely neutralized by bicarbonate. The most common etiologies of elevated anion gap acidoses can be remembered using the mnemonic MUDPILES: methanol, uremia, diabetic and alcoholic ketoacidosis, paraldehyde, isoniazid or iron, lactate, ethylene glycol, and salicylates (Box 1). A subsegment of these elevated anion gap acidoses are
Hyperchloremic or normal anion gap acidoses
The presence of a hyperchloremic or normal anion gap acidosis occurs by means of an excessive loss of HCO3− or an inability to excrete H+. HCO3− can be lost from the GI tract or from the kidneys, whereas, the inability to excrete H+ is a result of renal failure. More recent literature advocates calculation of a urinary anion gap (UAG) to aid in differentiating etiologies of an existing hyperchloremic acidosis. Although a negative UAG suggests GI HCO3− loss, a positive UAG indicates inability to
Summary
Although the presence and etiology of a metabolic acidosis in a tachypnic, dehydrated patient with a sweet odor on his or her breath and complaints of vomiting and polyuria is obvious, the physician is rarely so fortunate. More often, a metabolic acidosis must be confirmed by means of a simultaneous arterial blood gas and an electrolyte panel. Serum anion gap must be calculated to differentiate between an elevated gap and normal gap acidosis. The applicable mnemonic must be recalled, and each
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Management of an overdose patient
2020, Toxicology Cases for the Clinical and Forensic LaboratoryChanges in the SID<inf>Actual</inf> and SID <inf>Effective</inf> Values in the Course of Respiratory Acidosis in Horses With Symptomatic Severe Equine Asthma—An Experimental Study
2019, Journal of Equine Veterinary ScienceCitation Excerpt :This apparent lack of anions is known as the AG and is calculated according to the following formula: AG = ([Na+ mmol/L] + [K+ mmol/L]) − ([Cl−mmol/l]+ [HCO3−mmol/L]) [13,14]. In the course of metabolic acidosis, the value of AG usually increases [26], which is associated with a lower concentration, or “use” of HCO3− that binds H+ [19] from organic acids such as lactic, acetoacetic, and β hydroxybutyric acid [27]. For the clinician, the main disadvantage of the AG is that it does not take into account the concentration of albumin, a major blood protein buffer.
Approach to metabolic acidosis in the emergency department
2014, Emergency Medicine Clinics of North AmericaCitation Excerpt :In general, there are 2 mechanisms responsible: inadequate oxygen delivery and increased oxygen requirements. The most common cause in this category is shock, but also includes pulmonary disease, toxins, other causes of severe hypoxemia, anemia, and thromboembolic events.32 Type B lactic acidosis is a less-well understood entity whereby there is an increased lactate level with preserved oxygen delivery to tissues.
Falsely increased chloride and missed anion gap elevation during treatment with sodium thiosulfate
2014, Clinica Chimica ActaCitation Excerpt :In some cases this leads to severe acidosis associated with an increased anion gap, necessitating a decreased dose [3,4]. As the differential diagnoses of anion gap acidosis versus non-anion gap acidosis differ significantly, errors in chloride can lead to potentially dangerous diagnostic miscalculations and delays in treatment [16]. The prevalence of interference by STS is likely to increase, prompted by recognition of its effectiveness and increased use in the treatment of calciphylaxis [17].
Blood gas and acid-base analysis
2011, Anesthesia Secrets